ArticlePloS one2014
Osteopontin upregulates the expression of glucose transporters in osteosarcoma cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Osteopontin derived from hypoxia-induced M2 macrophages promotes osteosarcoma progression through modulation of EGR3/ISG15 signaling and RIG-I expression.Journal of translational medicine · 2025Article
- Osteopontin: A Key Multifaceted Regulator in Tumor Progression and Immunomodulation.Biomedicines · 2024Review
- Review
- Review
- Integrin signaling in cancer: bidirectional mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2023Review
- Metabolic reprogramming in osteosarcoma.Pediatric discovery · 2023Review
- Biological and Clinicopathological Characteristics of OPN in Cervical Cancers.Frontiers in genetics · 2022Article
- Endocrine regulation and metabolic mechanisms of osteopontin in the development and progression of osteosarcoma, metastasis and prognosis.Frontiers in endocrinology · 2022Review
- Uptake of fluorescent D- and L-glucose analogues, 2-NBDG and 2-NBDLG, into human osteosarcoma U2OS cells in a phloretin-inhibitable manner.Human cell · 2021Article
- Cancer metabolism and intervention therapy.Molecular biomedicine · 2021Review
- Adapt and conquer: Metabolic flexibility in cancer growth, invasion and evasion.Molecular metabolism · 2020Review
- Osteopontin in Bone Metabolism and Bone Diseases.Medical science monitor : international medical journal of experimental and clinical research · 2020Review
- The cancer-related transcription factor RUNX2 modulates expression and secretion of the matricellular protein osteopontin in osteosarcoma cells to promote adhesion to endothelial pulmonary cells and lung metastasis.Journal of cellular physiology · 2019Article
- Phloretin Suppresses Bone Morphogenetic Protein-2-Induced Osteoblastogenesis and Mineralization via Inhibition of Phosphatidylinositol 3-kinases/Akt Pathway.International journal of molecular sciences · 2019Article
- The Fate of Osteoblast-Like MG-63 Cells on Pre-Infected Bactericidal Nanostructured Titanium Surfaces.Materials (Basel, Switzerland) · 2019Article
- Osteopontin as a biomarker for osteosarcoma therapy and prognosis.Oncology letters · 2019Review
- Phloretin Promotes Adipogenesis via Mitogen-Activated Protein Kinase Pathways in Mouse Marrow Stromal ST2 Cells.International journal of molecular sciences · 2018Article
- Bone Cell Bioenergetics and Skeletal Energy Homeostasis.Physiological reviews · 2017Review
- Role of osteopontin in osteosarcoma.Medical oncology (Northwood, London, England) · 2015Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteosarcoma is the most common primary malignancy of bone. Even after the traditional standard surgical therapy, metastasis still occurs in a high percentage of patients. Glucose is an important source of metabolic energy for tumor proliferation and survival. Tumors usually overexpress glucose transporters, especially hypoxia-responsive glucose transporter 1 and glucose transporter 3. Osteopontin, hypoxia-responsive glucose transporter 1, and glucose transporter 3 are overexpressed in many types of tumors and have been linked to tumorigenesis and metastasis. In this study, we investigated the regulation of glucose transporters by osteopontin in osteosarcoma. We observed that both glucose transporters and osteopontin were upregulated in hypoxic human osteosarcoma cells. Endogenously released osteopontin regulated the expression of glucose transporter 1 and glucose transporter 3 in osteosarcoma and enhanced glucose uptake into cells via the αvβ3 integrin. Knockdown of osteopontin induced cell death in 20% of osteosarcoma cells. Phloretin, a glucose transporter inhibitor, also caused cell death by treatment alone. The phloretin-induced cell death was significantly enhanced in osteopontin knockdown osteosarcoma cells. Combination of a low dose of phloretin and chemotherapeutic drugs, such as daunomycin, 5-Fu, etoposide, and methotrexate, exhibited synergistic cytotoxic effects in three osteosarcoma cell lines. Inhibition of glucose transporters markedly potentiated the apoptotic sensitivity of chemotherapeutic drugs in osteosarcoma. These results indicate that the combination of a low dose of a glucose transporter inhibitor with cytotoxic drugs may be beneficial for treating osteosarcoma patients.
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